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The Role of CHMP4C on Proliferation in the Human Lung Cancer A549 Cells

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DOI: 10.4236/jct.2015.615133    4,062 Downloads   4,445 Views   Citations

ABSTRACT

The human lung cancer has high incidence rate and mortality among the carcinoma. The research on enhancing the efficacy of therapy for lung cancer is significant. A resent research found that as a subunit of ESCRT-III, CHMP4C functioned to retard abscission timing to coordinate midbody resolution and prevent accumulation of DNA damage in the abscission checkpoint through phosphorylated by AuroraB. In the current study, we evaluated the possible mechanism of the effects of CHMP4C inhibition on cell cycle and cell survival in A549 cells. We found that CHMP4C knockdown caused lagging S phase in cell cycle through enhancing the phosphorylation of Rb, raising the expression of cyclin B1-cdc2 and suppressing the activation of cyclin A. Meanwhile, CHMP4Cdeletion depressed cell survival via decreasing cell viability and increasing caspase 3/7 activity. This study may promote new significant reference and advance for the mechanism underlying specific function of CHMP4C as well as further research on enhancing therapy effect on non-small lung cancer.

Conflicts of Interest

The authors declare no conflicts of interest.

Cite this paper

Li, K. , Liu, J. , Tian, M. , Piao, C. , Ruan, J. , Gao, L. , Qi, X. , Gao, G. and Su, X. (2015) The Role of CHMP4C on Proliferation in the Human Lung Cancer A549 Cells. Journal of Cancer Therapy, 6, 1223-1228. doi: 10.4236/jct.2015.615133.

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